Abstract
Abstract: :
Purpose: Several lines of evidence implicate the IGF–1R in tumorigenesis. The IGF–1R is important for transformation and proliferation of malignant cells, preventing apoptosis, maintaining malignancy and protecting against chemotherapy, but IGF–1R is not critical for growth of normal cells. Recently we demonstrated that growth and survival of uveal melanoma cell lines are strongly dependent on IGF–1R expression and activation. These results raised the possibility of targeting IGF–1R in treatment of patients with uveal melanoma Methods: The uveal melanoma cell lines OCM–1 and OCM–3 were incubated with a small molecule, specifically inhibiting the IGF–1R tyrosine kinase. By densitometry the IGF–1R phosphorylation was quantified and cell death was assayed by colorimetric cell viability test. Results: Incubation of the cells with the inhibitor caused a dose–dependent decrease of IGF–1R phosphorylation with an IC50 value <500nM. IGF–1R inhibition was followed by a massive cell death. Conclusions: Our results open the possibility to use IGF–1R inhibitors as a therapeutic option for patients with uveal melanoma.
Keywords: oncology • uvea • melanoma